Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.
about
Rett Syndrome: Crossing the Threshold to Clinical TranslationExcitatory/Inhibitory Balance and Circuit Homeostasis in Autism Spectrum DisordersMeCP2 post-translational modifications: a mechanism to control its involvement in synaptic plasticity and homeostasis?Rett syndrome: disruption of epigenetic control of postnatal neurological functionsMethyl-CpG binding protein 2 (MeCP2) localizes at the centrosome and is required for proper mitotic spindle organizationMECP2 regulates cortical plasticity underlying a learned behaviour in adult female miceBeyond Widespread Mecp2 Deletions to Model Rett Syndrome: Conditional Spatio-Temporal Knockout, Single-Point Mutations and Transgenic Rescue MicePreclinical research in Rett syndrome: setting the foundation for translational success.The neural circuit basis of Rett syndromeFunctional recovery with recombinant human IGF1 treatment in a mouse model of Rett Syndrome.Systemic delivery of MeCP2 rescues behavioral and cellular deficits in female mouse models of Rett syndromeMeCP2 dependent heterochromatin reorganization during neural differentiation of a novel Mecp2-deficient embryonic stem cell reporter line.Gait analysis in a Mecp2 knockout mouse model of Rett syndrome reveals early-onset and progressive motor deficitsMouse models of neurodevelopmental disease of the basal ganglia and associated circuits.The molecular basis of variable phenotypic severity among common missense mutations causing Rett syndromeHuman-specific regulation of MeCP2 levels in fetal brains by microRNA miR-483-5p.NMDA receptor regulation prevents regression of visual cortical function in the absence of Mecp2.Acute and crucial requirement for MeCP2 function upon transition from early to late adult stages of brain maturationLoss of MeCP2 function is associated with distinct gene expression changes in the striatumBreathing challenges in Rett syndrome: lessons learned from humans and animal models.Oligodendrocyte lineage cells contribute unique features to Rett syndrome neuropathologyRescue of behavioral and EEG deficits in male and female Mecp2-deficient mice by delayed Mecp2 gene reactivation.From Function to Phenotype: Impaired DNA Binding and Clustering Correlates with Clinical Severity in Males with Missense Mutations in MECP2.Loss of MeCP2 from forebrain excitatory neurons leads to cortical hyperexcitation and seizures.Synaptic plasticity and signaling in Rett syndrome.Rett syndrome: a complex disorder with simple roots.Defects During Mecp2 Null Embryonic Cortex Development Precede the Onset of Overt Neurological Symptoms.The 3' UTR of FMR1 mRNA is a target of miR-101, miR-129-5p and miR-221: implications for the molecular pathology of FXTAS at the synapse.Radically truncated MeCP2 rescues Rett syndrome-like neurological defects.Selective preservation of MeCP2 in catecholaminergic cells is sufficient to improve the behavioral phenotype of male and female Mecp2-deficient mice.Expression of Phospho-MeCP2s in the Developing Rat Brain and Function of Postnatal MeCP2 in Cerebellar Neural Cell Development.Conditional depletion of methyl-CpG-binding protein 2 in astrocytes depresses the hypercapnic ventilatory response in mice.A mutation-led search for novel functional domains in MeCP2.
P2860
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P2860
Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.
description
2012 nî lūn-bûn
@nan
2012 թուականի Մայիսին հրատարակուած գիտական յօդուած
@hyw
2012 թվականի մայիսին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
name
Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.
@ast
Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.
@en
Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.
@nl
type
label
Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.
@ast
Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.
@en
Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.
@nl
prefLabel
Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.
@ast
Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.
@en
Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.
@nl
P2093
P2860
P356
P1476
Postnatal inactivation reveals enhanced requirement for MeCP2 at distinct age windows.
@en
P2093
Adrian Bird
Cara Merusi
Dina De Sousa
Hélène Cheval
Jim Selfridge
P2860
P304
P356
10.1093/HMG/DDS208
P577
2012-05-31T00:00:00Z